Asunto(s)
Cardiomiopatía Chagásica , Enfermedad de Chagas , Trasplante de Corazón , Miocarditis , Trypanosoma cruzi , Humanos , Miocarditis/diagnóstico , Enfermedad de Chagas/diagnóstico , Enfermedad de Chagas/parasitología , Trasplante de Corazón/efectos adversos , Biopsia , Carga de Parásitos , Cardiomiopatía Chagásica/patologíaRESUMEN
BACKGROUND: Chagas disease reactivation (CDR) after heart transplantation is characterized by relapse of the infectious disease with proliferation and dissemination of Trypanosoma cruzi parasites. Serial blood PCR testing is consensually recommended for CDR monitoring, but there is uncertainty about the incremental value in performing the molecular tests in endomyocardial biopsies (EMB). METHODS: We compared qualitative and quantitative results of PCR for T cruzi DNA in 62 pairs of blood and EMB collected with a maximum time interval of 7 days, from 34 heart-transplanted, chagasic patients. RESULTS: Blood PCR resulted positive in 39/62 (62.9%) samples, with PL ranging from 0.14 to 1610.73 (median: 3.31). PCR resulted positive in 8/60 (13.3%) EMB, with PL ranging from 2.82 to 1670.55 (median: 65.63). All blood samples which tested negative presented a paired EMB which also tested negative. However, 31/39 (79.5%) blood samples which tested positive presented a paired EMB which tested negative. There was poor agreement between blood and EMB PCR (kappa = 0.153). CDR affecting the myocardium (myo-CDR) was diagnosed in three occasions. PCR resulted positive in both blood and EMB at the time of myo-CDR, with PL ranging from 0.61 to 1610.73 in blood and 13.8 to 1670.55 in EMB. CONCLUSIONS: Negative PCR for T cruzi in blood rules out myo-CDR, with no value of testing EMB. Positive PCR in blood with high PL is diagnostic for myo-CDR. If PCR in blood results positive with low PL, testing EMB is useful: negative PCR turns unlikely, and positive PCR reinforces greatly the possibility of myo-CDR.
Asunto(s)
Enfermedad de Chagas , Trasplante de Corazón , Trypanosoma cruzi , Biopsia , Enfermedad de Chagas/diagnóstico , ADN , Endocardio , Trasplante de Corazón/efectos adversos , Humanos , Reacción en Cadena de la Polimerasa , Trypanosoma cruzi/genéticaAsunto(s)
Estenosis Coronaria/terapia , Vasos Coronarios/patología , Embolia/patología , Cuerpos Extraños/patología , Microvasos/patología , Intervención Coronaria Percutánea/instrumentación , Anciano , Resultado Fatal , Cuerpos Extraños/complicaciones , Migración de Cuerpo Extraño/patología , Humanos , Interacciones Hidrofóbicas e Hidrofílicas , Riñón/patología , Masculino , Persona de Mediana Edad , Infarto del Miocardio con Elevación del ST , Choque Cardiogénico/etiologíaRESUMEN
BACKGROUND: Chagas' disease (CD) is caused by infection with the protozoan Trypanosoma cruzi. The disease can affect the heart and/or the gastrointestinal (GI) tract, but around 70% of infected individuals remain asymptomatic in the chronic form. Organ transplantation from T. cruzi-infected donors is often avoided because of the risk of disease transmission, previously reported after heart, kidney, or liver transplantation. METHODS: We investigated by histology, immunohistochemistry, and polymerase chain reaction (PCR) the persistence of T. cruzi in samples of the heart, lung, liver, kidney, pancreas, adrenal gland, esophagus, and GI tract of 21 chronic chagasic patients. RESULTS: Parasite persistence was detected in 12/21 (57.1%) heart samples, mainly by PCR-based assays. T. cruzi parasites were detected by histology and immunohistochemistry in smooth muscle cells of the central vein from 1/21 (4.8%) adrenal gland samples. No samples of the lung, liver, kidney, pancreas, esophagus, or GI tract were found to have parasites by histology, immunohistochemistry, or PCR. CONCLUSIONS: We concluded that, aside from the heart, the other solid organs of T. cruzi-infected donors can be used for transplantation with a lot of caution. Such organs are not safe in the view of previous reports of CD transmission, but seem to present a low T. cruzi load compared to the heart.
Asunto(s)
Enfermedad de Chagas/patología , Transmisión de Enfermedad Infecciosa/prevención & control , Trasplante de Órganos/efectos adversos , Obtención de Tejidos y Órganos/métodos , Trypanosoma cruzi/aislamiento & purificación , Adulto , Anciano , Animales , Infecciones Asintomáticas , Enfermedad de Chagas/parasitología , Enfermedad de Chagas/transmisión , ADN Protozoario/aislamiento & purificación , Femenino , Corazón/parasitología , Humanos , Inmunohistoquímica , Masculino , Persona de Mediana Edad , Miocardio/patología , Trasplante de Órganos/métodos , Reacción en Cadena de la Polimerasa , Trypanosoma cruzi/genética , Adulto JovenRESUMEN
BACKGROUND: Chagas' disease reactivation (CDR) after heart transplantation is characterized by relapse of the infectious disease, with direct detection of Trypanosoma cruzi parasites in blood, cerebrospinal fluid, or tissues. CDR affecting the myocardium induces lymphocytic myocarditis and should be distinguished from acute cellular rejection in endomyocardial biopsy (EMB) specimens. METHODS: We performed retrospectively qualitative polymerase chain reaction for T cruzi DNA using 2 sets of primers targeting nuclear DNA (nDNA) or kinetoplast DNA (kDNA) in 61 EMB specimens of 11 chagasic heart transplant recipients who presented with CDR. Thirty-five EMB specimens were obtained up to 6 months before (pre-CDR group) and 26 up to 2 years after the diagnosis of CDR. The control group consisted of 6 chagasic heart transplant recipients with 18 EMB specimens who never experienced CDR. RESULTS: Amplification of kDNA occurred in 8 of 35 (22.9%) EMB specimens of the pre-CDR group, in 5 of 18 (27.8%) of the control group, and in 17 of 26 (65.4%) EMB specimens obtained after the successful treatment of CDR. Amplification of nDNA occurred in 3 of 35 (8.6%) EMB specimens of the pre-CDR group, 0 of 18 (0%) of the control group, and 6 of 26 (23.1%) EMB specimens obtained after the successful treatment of CDR. CONCLUSIONS: Amplification of kDNA in EMB specimens is not specific for the diagnosis of CDR, occurring also in patients with no evidence of CDR (control group). However, amplification of nDNA occurred in a few EMB specimens obtained before CDR, but in none of the control group specimens. Qualitative PCR for T cruzi DNA in EMB specimens should not be used as a criterion for cure of CDR because it can persist positive despite favorable clinical evolution of the patients.
Asunto(s)
Enfermedad de Chagas/diagnóstico , ADN Protozoario/análisis , Trasplante de Corazón/efectos adversos , Reacción en Cadena de la Polimerasa/métodos , Trypanosoma cruzi/aislamiento & purificación , Adolescente , Adulto , Estudios de Casos y Controles , Núcleo Celular , Enfermedad de Chagas/parasitología , Enfermedad de Chagas/cirugía , ADN de Cinetoplasto/análisis , Endocardio/parasitología , Femenino , Corazón/parasitología , Humanos , Masculino , Persona de Mediana Edad , Miocardio , Recurrencia , Estudios Retrospectivos , Trypanosoma cruzi/genética , Adulto JovenRESUMEN
BACKGROUND: Endocardial fibrous tissue (FT) deposition is a hallmark of endomyocardial fibrosis (EMF). Echocardiography is a first-line and the standard technique for the diagnosis of this disease. Although late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) allows FT characterization, its role in the diagnosis and prognosis of EMF has not been investigated. METHODS AND RESULTS: Thirty-six patients (29 women; age, 54±12 years) with EMF diagnosis after clinical evaluation and comprehensive 2-dimensional Doppler echocardiography underwent cine-CMR for assessing ventricular volumes, ejection fraction and mass, and LGE-CMR for FT characterization and quantification. Indexed FT volume (FT/body surface area) was calculated after planimetry of the 8 to 12 slices obtained in the short-axis view at end-diastole (mL/m(2)). Surgical resection of FT was performed in 16 patients. In all patients, areas of LGE were confined to the endocardium, frequently as a continuous streak from the inflow tract extending to the apex, where it was usually most prominent. There was a relation between increased FT/body surface area and worse New York Heart Association functional class and with increased probability of surgery (P<0.05). The histopathologic examination of resected FT showed typical features of EMF with extensive endocardial fibrous thickening, proliferation of small vessels, and scarce inflammatory infiltrate. In multivariate analysis, the patients with FT/body surface area >19 mL/m(2) had an increased mortality rate, with a relative risk of 10.8. CONCLUSIONS: Our study provides evidence that LGE-CMR is useful in the diagnosis and prognosis of EMF through quantification of the typical pattern of FT deposition.
Asunto(s)
Medios de Contraste , Fibrosis Endomiocárdica/diagnóstico , Gadolinio DTPA , Imagen por Resonancia Magnética , Adulto , Anciano , Fibrosis Endomiocárdica/complicaciones , Fibrosis Endomiocárdica/patología , Fibrosis Endomiocárdica/fisiopatología , Femenino , Insuficiencia Cardíaca/complicaciones , Ventrículos Cardíacos/patología , Humanos , Procesamiento de Imagen Asistido por Computador , Imagen por Resonancia Cinemagnética , Masculino , Persona de Mediana Edad , Pronóstico , Volumen SistólicoRESUMEN
Pain is the most conspicuous symptom observed in patients wounded by stingrays, and skin necrosis is common in accidents by freshwater stingrays. The extract from the stinger integumentary tissue of Potamotrygon falkneri containing toxic components (venom) was tested for its ability to induce histopathological changes in the dorsal skin of mice at different times. 3-6 h after injection, foci of necrosis in isolated basal epidermal cells were observed. Full coagulative necrosis of the skin, subcutaneous tissue and skeletal muscle was evident as soon as 24 h after venom exposure, with a clear demarcation from the normal skin. After 48 h, round collections of necrotic cells start to coalesce originating extensive skin necrotic plaques that detach from viable tissue after 72-96 h. Inflammatory infiltrate was observed after 6 h, but was always mild. Acute vascular thrombosis was rare, and hemorrhage was not present at any time. Superficial bacterial infection was present in two of the examined cases. In conclusion, the venom of P. falkneri is responsible for the development of an early necrosis with mild inflammatory reaction, probably due to direct action of the venom. The severe local damage is probably worsened by the mechanical trauma caused by the stinger.
Asunto(s)
Venenos de los Peces/toxicidad , Rajidae , Piel/patología , Animales , Ratones , NecrosisRESUMEN
Pain is the most conspicuous symptom observed in patients wounded by stingrays, and skin necrosis is common in accidents by freshwater stingrays. The extract from the stinger integumentary tissue of Potamotrygon falkneri containing toxic components (venom) was tested for its ability to induce histopathological changes in the dorsal skin of mice at different times. 3-6 h after injection, foci of necrosis in isolated basal epidermal cells were observed. Full coagulative necrosis of the skin, subcutaneous tissue and skeletal muscle was evident as soon as 24 h after venom exposure, with a clear demarcation from the normal skin. After 48 h, round collections of necrotic cells start to coalesce originating extensive skin necrotic plaques that detach from viable tissue after 72-96 h. Inflammatory infiltrate was observed after 6 h, but was always mild. Acute vascular thrombosis was rare, and hemorrhage was not present at any time. Superficial bacterial infection was present in two of the examined cases. In conclusion, the venom of P. falkneri is responsible for the development of an early necrosis with mild inflammatory reaction, probably due to direct action of the venom. The severe local damage is probably worsened by the mechanical trauma caused by the stinger.
Asunto(s)
Masculino , Femenino , Humanos , Animales , Rajidae/clasificación , Toxinas MarinasRESUMEN
Isolated noncompaction of the myocardium (INCM) is a rare, congenital, unclassified cardiomyopathy. It is caused by a disorder in endomyocardial morphogenesis in the absence of other structural disease. INCM is characterized by numerous prominent trabeculations and deep intertrabecular recesses in the myocardium. Frequently, INCM is associated with an increased incidence of heart failure, arrhythmias, and cardioembolic events with high morbidity and mortality. We describe a 28-year-old woman experiencing symptoms of heart failure since she was 4 years old. She had been intensively investigated and misdiagnosed as having dilated, restrictive, and apical hypertrophic cardiomyopathies. Cardiac magnetic resonance and echocardiography recently revealed the actual diagnosis of INCM. The patient is alive and well, taking vasodilators and warfarin. Herein, we describe the long-term follow-up of this patient and demonstrate that some patients have a favorable prognosis. In addition, the improvement in noninvasive cardiac imaging has revealed a higher prevalence of INCM, previously undetected.
Asunto(s)
Cardiomiopatías/congénito , Cardiomiopatías/diagnóstico por imagen , Disfunción Ventricular Izquierda/congénito , Disfunción Ventricular Izquierda/diagnóstico por imagen , Anticoagulantes/uso terapéutico , Cardiomiopatías/tratamiento farmacológico , Preescolar , Diagnóstico Diferencial , Femenino , Humanos , Estudios Longitudinales , Análisis de Supervivencia , Factores de Tiempo , Ultrasonografía , Vasodilatadores/uso terapéutico , Disfunción Ventricular Izquierda/tratamiento farmacológico , Warfarina/uso terapéuticoRESUMEN
A 36-year old woman was bitten on the left ankle by a Bothrops jararacussu, and died 45 min after the bite. At necropsy, there were local signs of envenoming with haemorrhage, thrombosis and necrosis of the subcutaneous and muscular tissue. Multiple fibrin and platelet thrombi were found in the microcirculation of the heart and lungs, suggesting the occurrence of disseminated intravascular coagulation. Pulmonary haemorrhage probably secondary to the action of haemorrhagins, consumption coagulopathy and disseminated intravascular coagulation was the immediate cause of death. Intravenous inoculation of the venom could have occurred in the present case, which would explain the rapid onset of coagulation disorders, haemorrhage and death.
Asunto(s)
Bothrops , Coagulación Intravascular Diseminada/etiología , Hemorragia/etiología , Enfermedades Pulmonares/etiología , Mordeduras de Serpientes/complicaciones , Adulto , Animales , Autopsia , Coagulación Intravascular Diseminada/patología , Resultado Fatal , Femenino , Humanos , Mordeduras de Serpientes/patología , Venenos de Serpiente/envenenamientoRESUMEN
BACKGROUND: The ventricles of the normal heart are virtually devoid of atrial natriuretic peptide (ANP). Although ANP occurs in ventricles submitted to elevated wall stress, it is not clear whether ANP expression is affected by myocarditis. We investigated the immunohistochemical expression of ANP in chronic chagasic cardiomyopathy, an inflammatory cardiomyopathy caused by infection with the protozoan Trypanosoma cruzi. METHODS: Necropsy samples from the left and right ventricles of 16 patients exhibiting chronic chagasic cardiomyopathy were evaluated for myocarditis, fibrosis, T. cruzi parasites and ANP immunoreactivity. The diameters of 50 myocytes per sample were measured. RESULTS: ANP was present in myocytes of the subendocardial region in 13/16 (81.3%) left and 10/16 (62.5%) right ventricular samples (P=0.25). Myocytes present in the inflammatory foci, near the infiltrating inflammatory cells but distant from the subendocardial region, did not express ANP. Trypanosoma cruzi parasites exhibited intense immunoreactivity for ANP. The mean myocyte diameter and the incidence of myocarditis, fibrosis, and T. cruzi parasites was similar between the left and right ventricular samples. No statistical differences were found between the ANP-positive and ANP-negative cases. CONCLUSIONS: In chronic chagasic cardiomyopathy, both ventricles exhibit hypertrophy, fibrosis and ANP in the subendocardial region. The inflammatory infiltrate does not induce ANP expression in the myocytes. Regional stress but not myocarditis itself, is probably responsible for ventricular ANP expression in myocarditis.